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Published on: February 14, 2016
A systems-level proteomic analysis identifies kinesin targets of KIFBP during neuronal development
Biorxiv : the Preprint Server for Biology
|August 1, 2026
Summary
Kinesin family binding protein (KIFBP) is crucial for neuronal development. Loss of KIFBP impairs neurite extension by affecting kinesin motor proteins, offering insights into neurodevelopmental disorders.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Kinesins are motor proteins vital for neuronal cytoskeleton organization.
- Kinesin family binding protein (KIFBP) regulates kinesins by blocking microtubule interactions.
- KIFBP mutations cause Goldberg-Shprintzen Syndrome (GOSHS), a neurodevelopmental disorder.
Purpose of the Study:
- To investigate the specific kinesins regulated by KIFBP.
- To understand KIFBP's role in neurite extension and neuronal differentiation.
- To identify novel KIFBP targets in neuronal development.
Main Methods:
- CRISPR-Cas9 KIFBP knockout in Neuro-2a cells.
- Inducible GFP-KIFBP expression for interactome studies.
- Immunoprecipitation, mass spectrometry, and single-molecule TIRF microscopy.
Main Results:
- KIFBP is essential for neurite extension in Neuro-2a cells.
- Identified known and novel kinesin interactors of KIFBP.
- Confirmed direct inhibition of a subset of kinesins by KIFBP.
- Identified KIF5A and KIF18B as new regulatory targets.
Conclusions:
- Neuro-2a cells serve as a model for KIFBP research.
- KIFBP regulates kinesin activity and cytoskeletal dynamics in neurons.
- Findings provide new insights into GOSHS pathogenesis and neuronal development.
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